Atherosclerotic plaques: is endothelial shear stress the only factor?
Related Experiment Video
Updated: May 11, 2026

Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice
Published on: January 13, 2012
Afshin Anssari-Benam1, Theodosios Korakianitis
1Faculty of Engineering Sciences, University College London, Torrington Place, London WC1E 7JE, UK. a.anssari-benam@ucl.ac.uk
Insights
Atherosclerosis may be caused by more than just irregular shear stress. New research suggests the combined effects of wall shear stress and circumferential stress waves, indicated by angular phase difference, could be key to plaque development.
Area of Science:
- Cardiovascular science
- Biomedical engineering
- Mechanobiology
Background:
- Atherosclerosis initiation is often linked to abnormal shear stress patterns.
- Clinical evidence suggests plaque formation occurs even in areas with steady, high shear stress, challenging current theories.
- This indicates other hemodynamic factors beyond shear stress may contribute to atherosclerosis.
Purpose of the Study:
- To propose a new hypothesis for atherosclerosis development.
- To investigate the combined effect of wall shear stress and circumferential stress waves.
- To identify the angular phase difference as a potential determinant of plaque formation.
Main Methods:
- Review of existing literature on atherosclerosis and hemodynamics.
- Formulation of a hypothesis based on combined hemodynamic forces.
- Theoretical analysis of the angular phase difference between shear stress and circumferential stress waves.
Main Results:
- Current models attributing atherosclerosis solely to shear stress may be incomplete.
- A novel hypothesis suggests the angular phase difference between wall shear stress and circumferential stress waves is a critical factor.
- Positive angular phase difference values may correlate with increased plaque formation risk.
Conclusions:
- Deviations from normal shear stress alone are insufficient to explain atherosclerosis.
- The interplay between wall shear stress and circumferential stress waves, quantified by angular phase difference, offers a more comprehensive explanation.
- This theory could revolutionize understanding of endothelial mechanotransduction and lead to new diagnostic tools.
Abstract:
Initiation and development of atherosclerosis has largely been attributed to irregular shear stress patterns and values, in the current literature. Abnormalities such as low shear stress, reversing and oscillatory shear force patterns, as well as temporal variations of shear stress are the most cited factors. However, clinical findings have further indicated that plaques have still been formed and developed in arterial sites that possess relatively more steady and higher shear stresses than those observed in studies correlating low or oscillatory shear stresses with atherosclerosis. These data imply that deviations in shear stress from its normal physiological pattern alone may not be the only factor inducing atherosclerosis, and additional haemodynamics parameter other then shear stress may also contribute to the initiation and development of plaques. In this paper, we hypothesise that the combined effect of wall shear stress and circumferential stress waves, in the form of angular phase difference between the two waves at each cardiac cycle, may be a more accurate determinant of plaque formation and growth. Furthermore, arterial sites that possess more positive values of this angular phase difference may be more prone to plaque formation or development. If proved correct, this theory can transform our understanding of endothelial cell mechanotransduction and mechanobiology, and may lead to design and utilisation of new diagnostic procedures and equipment as predictive and preventive clinical tools for patients with abnormal arterial blood pressure.
Related Concept Videos
Atherosclerosis I: Introduction
Coronary Artery Disease II: Pathophysiology
Peripheral Artery Disease I: Introduction
Coronary Artery Disease I: Introduction
Atherosclerosis III: Management
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests

